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SRNAPharmacology II > HIstamine receptors Blockers-COMP > Flashcards

HIstamine receptors Blockers-COMP Flashcards

1
Q

Histamine is a natural occurring

Does histamine cross the BBB?

A

Amine

- Does not cross the BBB

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2
Q

Histamine and inflammation

Found where?

A

Act as a mediator for inflammation in allergic disease

- Found in mast cells of skin. lungs and GIT

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3
Q

H1 receptors does what?

H2 receptors does what?

A

H1- Smooth muscle contraction in respiratory and GI tract

H2- Increase myocardial contractility and Heart

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4
Q

H3 receptors

A

cause inhibition, synthesis and release of histamine

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5
Q

Activitiy of H3 receptors may be

A

Impaired by H2 receptors.

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6
Q

Impairment of H3 receptors by H2 antagonists may result in an

A

Increase relase of histamine when a drug that cause histamine is given to a patient that was pre-treated with H2 antagonist alone

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7
Q

Histamine profound effect of

A

CV, airways and gastric H+ ions

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8
Q

Does histamine cross BBB

A

no

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9
Q

Predominant CV effect of histamine

A

Dilation of arterioles and capillaries leading to flushing decrease in PVR and Systemic BP and increase capillary permeability

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10
Q

Vascular effects are from direct effect of histamine on

A

Blood vessels mediated by H1 and H2

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11
Q

H2 receptor are activated at higher histamine concentrations

A

Slower onset and result in sustained vasodilation

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12
Q

H2 on conduction

A

Slow conduction of cardiac impulses through the AV node due to activation of H1 receptors

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13
Q

Zantac too quickly

A

Arrythmias

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14
Q

Positive chronotropic, inotropic effects and cardiac dysrhythmias are due to activation of

A

H2 receptors in the heart as well as the release of catecholamines from the adrenal medulla

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15
Q

Histamine in LARGE DOSES stimulates_____and_________ in the adrenal medulla, evoking the release of catecholamines.

A

ganglion cells and chromaffin cells

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16
Q

Pt with obstructive airway disease such as

A

Asthma and bronchitis are more likely to develop an increase in airway resistance in response to histamine

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17
Q

For AnTICHOLINERGIC and gastric secretions

A

high doses to affect GI secretions

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18
Q

Cholinergic blockade

A

Decrease the gastric secretory response to histamine

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19
Q

Bronchoconstriction is

A

Not prevented

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20
Q

Clinical use of the drug

A

Assess ability of gastric pariety cells to secrete H+

to determine parietal cell mass

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21
Q

Histamine with zollinger ellison

A

Hypersecretion of H+ ions in response to histamine in presence with zollinger ellison syndrome.

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22
Q

Histamine Receptor Antagonists

A

Class H1 or class H2

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23
Q

Histamine Receptor Antagonists act by

A

occupying receptors on effector cell membranes.

• For antihistamines this is a competitive and reversible interaction.

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24
Q

• H1 and H2 do not

A

inhibit the release of histamine.

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25
Q

H1 Receptor antagonist classified as

A

1st and 2nd generation

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26
Q

At low concentratons H1 antagonist act as

A

Competitive ANTAGONISTS

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27
Q

Most antihistamines are metabolized by:

A

hepatic microsomal enzymes.

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28
Q

Anticholinergic effects include;

A

dry mouth, blurred vision, urinary retention, and impotence may occur.

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29
Q

CNS effects of 1st generation

A

Sedation

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30
Q

CNS effects of 2nd generation

A

Non sedation

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31
Q

First generation H1 antagonist may also block

A

muscarinic cholinergic, 5-hydroxytryptomine (serotonin), or alpha-adrenergic receptors.

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32
Q

Levaquin

A

Can prolong QT

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33
Q

Short duration of Action

A

Benadryl

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34
Q

Most potent

A

Famodidine (Pepcid)

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35
Q

Least potent

A

(Cimetidine) Tagammet

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36
Q

Histamine and vascular endothelium to

A

stimulate release nitric oxide, which stimulates guanylate cyclase to increase levels of GMP in vascular smooth muscle, causing vasodilation

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37
Q

The release of prostacyclin from vascular endothelium is mediated by which receptor?

A

H1 receptors

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38
Q

Histamine activates the enzyme ________which leads to the release of ________

A

phospholipase; prostacyclin

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39
Q

The histamine-induced effects mediated by H1 receptors are

A

blocked by H1 receptor blockers.

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40
Q

Vascular effects of histamine are mediated by

A

H1 and H2 receptors

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41
Q

Which receptors are activated at lower concentrations?

A

H1 receptors: effects rapid and transient

42
Q

Which receptors are activated at Higher concentrations?

A

H2 receptors

43
Q

Slowed conduction of cardiac impulses through the AV node is due to

A

activation of H1 receptors.

44
Q

Coronary artery vasoconstriction is mediated by and

A

H1 receptors,

45
Q

Coronary artery vasodilation is mediated by

A

H2 receptors.

46
Q

Decrease in systemic BP induced by histamine are prevented by

A

prior administration of the combination of H1 and H2 receptor antagonist.

47
Q

Blocking either receptor alone

A

does not completely prevent the hypotensive effects of histamine

48
Q

The presence of vagal activity results in even higher rate

A

hydrogen ion secretion.

49
Q

Anacidity or hyposecretion of hydrogen ions in response to histamine may reflect

A

pernicious anemia, atrophic gastritis or gastric carcinoma.

50
Q

At low concentrations H1 antagonist act as

A

competitive antagonist.

51
Q

At high concentrations second generation H1 antagonist can act as

A

non-competitive antagonist.

52
Q

H2 antagonists with mild sedative effects

A

Cimetidine

53
Q

H1 Antagonists Marked anticholinergic effects

A

Benadryl (diphenhydramine)

Phenergan (Promethazine)

54
Q

H1 antagonists with marked SEDATIVE effects

A

Benadryl (diphenhydramine)

55
Q

H1 antagonists with marked ANTIEMETIC effects

A

Promethazine (Phenergan)

56
Q

H1 antagonists with MODERATE ANTIEMETIC effects

A

Diphenhydramine (Benadryl)

57
Q

Promethazine (Phenergan) Duration of action

A

4 to 24 hours

58
Q

H2 antagonists medications are

A

Cimetidine, ranitidine, famotidine, and nizatidine

59
Q

H2 antagonists are _______and _______inhibition of

A

that produce selective and reversible inhibition of H2 mediated secretion of acidic gastric fluid.

60
Q

The histamine receptors on membranes of the acid-secreting parietal cells are of the ___type and are therefore not blocked by____ antagonists

A

H2; H1 antagonist

61
Q

The occupation of H2 receptors by histamine released by mast cells and possibly other cells

A

activates adenylate cyclase, increasing the concentration of cAMP.

62
Q

The occupation of H2 receptors, The increase in cAMP activates the

A

proton pump of the gastric parietal cells to secrete hydrogen ions against a large concentration gradient

63
Q

The principal method of clearance from the plasma of oral doses of cimetidine, ranitidine, and famotidine

A

Hepatic metabolism

64
Q

Renal clearance is the principal method for oral

doses of

A

nizatidine

65
Q

The dose of cimetidine should be decreases in

A

patients with hepatic disease to avoid mental confusion.

66
Q

Renal failure increases the elimination half life of

A

the H2 antagonist with the greatest effect on famotidine and nizatidine.

67
Q

Decreases in dose are recommended for all of the

A

H2 antagonist for patients with renal failure.

68
Q

Duodenal ulcers associated with

A

hypersecretion of gastric hydrogen ions.

69
Q

In the preoperative period H2 antagonist are used to

A

increase the pH of gastric fluid before induction of anesthesia.

70
Q

H2 antagonist are useful agents to decrease the risk of .

A

acid pneumonitis if inhalation of acidic gastric fluid occurs in the perioperative period

71
Q

___________prior to induction, with or without a similar dose the evening prior to surgery.

A

Cimetidine 300mg orally 1.5-2 hours

72
Q

H-2 antagonist ability to decrease the

A

volume of gastric fluid has been unpredictable

73
Q

H2 antagonist have no influence on the

A

pH of the fluid already present in the stomach

74
Q

Preoperative preparation of patients with allergic histories or patients undergoing procedures with an increase likelihood of allergic reactions (radiographic contrast dyes) may include prophylactic oral administration of an

A 
H1 antagonist ( diphenhydramine 0.5-1mg/kg) AND an 
H2 antagonist (cimetidine 4mg/kg) every 6 hours in the 12 to 24 hour period prior to the event
75
Q

H2 antagonist can be used in combination with an H1 antagonist to prevent the effects of histamine releasing drugs such as

A

morphine or atracurium, mivacurium, or protamine.

76
Q

H2 antagonists Most common side effects include

A

diarrhea, headache, fatigue, and muscle pain

77
Q

_______and _______ are associated with rapid IV administration of these agents most often to the elderly of critically ill.

A

Bradycardia and hypotension

78
Q

Numerous drug interactions have been described between H-2 antagonist .

A

most commonly cimetidine. •

79
Q

H2 antagonists The principal mechanism is impairment of

A

hepatic microsomal (cytochrome p-450) enzymes by cimetidine.

80
Q

Cimetidine inhibits metabolism of drugs such as

A

propranolol, and diazepam that undergo high hepatic extraction.

81
Q

Drugs that eliminated byare not effected

A

conjugation (oxazepam, lorazepam)

82
Q

Cimetidine may increase the toxicity of

A

lidocaine

83
Q

Cimetidine modestly decreases_________ and

A

deflurination of methoxyflurane; inhibits oxidative metabolism of halothane.

84
Q

Ranitidine has less potential than cimetidine to alter

A

hepatic enzymes.

85
Q

Famotidine and nizatidine do not

A

bind to hepatic enzymes

86
Q

Cimetidine and ranitidine can impair renal tubular secretion of

A

procainamide and theophylline.

87
Q

Magnesium and aluminum containing antacids can

A

decrease the absorption of the H2 antagonist.

88
Q

Proton Pump Inhibitors

A

Drugs that provides prolonged inhibition of gastric acid secretion, regardless of the stimulus.

89
Q

PPI These agents work by:

A

inhibiting gastric parietal cell hydrogen-potassium ATPase (PPI).

90
Q

Daytime and nocturnal acid secretion and meal

A

stimulated acid secretion are inhibited to a greater degree with PPI then with H2 antagonist.

91
Q

Currently the best treatment for Zollinger-Ellison syndrome.

A

PPI

92
Q

Lansoprazole is available in a

A

suspension form

93
Q

Pantoprazole is available in

A

IV formulation.

94
Q

Omeprazole or esomeprazole capsules can be opened and the

A

granules can be placed into sodium bicarbonate.

95
Q

Most common adverse reactions of PPI include; –

A

headache, and diarrhea

96
Q

Serious but rare adverse reactions include

A 
– Blood	dyscrasia	
– Hepatic dysfunction	
– Stevens Johnson	syndrome	
– Erythema	multiforme	
– Pancreatitis
97
Q

Studies with omeprazole suggest that this agent should be given

A

> 3 hours prior to induction of anesthesia in order to be effective.

98
Q

Cromolyn inhibits antigen-induced release of histamine and other autacoids, including

A

leukotrienes from pulmonary mast cells, as well as from mast cells at other sites.

99
Q

Cromolyn is used in the prophylactic treatment of asthma and has

A

no role in the treatment of an acute asthmatic attack.

100
Q

Cromolyn does not

A

prevent the release of histamine from basophils, and cromolyn does not relax bronchial or vascular smooth muscle

SRNAPharmacology II (32 decks)

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